Gastrulation in C. elegans is normally initiated by the inward migration of the two gut precursor (E) cells at the 26-cell stage. We have isolated a gastrulation defective, temperature sensitive mutation, ct226ts, defining a gene called gad-1 (gastrulation defective).ct226ts exhibits a strict maternal effect, and appears to be a hypomorphic allele. At 25C, self-progeny embryos from homozygous hermaphrodites fail to initiate gastrulation Instead, their E cells divide early and in the wrong plane, and do not migrate into the embryo. Embryos continue to develop and undergo differentiation of all the major cell types, but do not undergo morphogenesis. We have rescued gad-1 homozygous mutant animals by injecting a subclone of genomic DNA containing only one complete gene. Its predicted translation product is similar to the beta-transducin family of G protein beta -subunits and contains 6 WD-repeats, suggesting that the protein plays a regulatory role. These sequences have b een investigated using the MEME/MAST server. We are currently isolating the cDNA, after which we will look for the molecular lesion in ct226 animals. We will also make reporter constructs to ascertain where the gene is expressed. Other maternal-effect genes with similar defective phenotypes have been identified (but not characterized), and embryonic transcription is also required for gastrulation initiation (Powell-Coffman, Knight and Wood, 1996, Dev. Biol. 178, 472-483). We will be working on how these other genes may interact together or separately to control gastrulation. Ultimately, we hope to ascertain whether the gad-1 gene product is a component of a signaling pathway that controls gastrulation initiation.